Ferroptosis is a type of regulated cell death (RCD) that plays a significant role in the pathogenesis of cardiovascular diseases (CVDs). It is characterized by iron-dependent lipid peroxidation and the accumulation of reactive oxygen species (ROS). Ferroptosis is involved in various CVDs, including myocardial infarction, heart failure, atherosclerosis, and pulmonary arterial hypertension. The mechanisms of ferroptosis involve iron metabolism, glutathione metabolism, and lipid metabolism. Recent research has shown that ferroptosis is involved in the occurrence and development of CVDs, and understanding its mechanisms can provide new ideas and treatment targets for the clinical diagnosis and treatment of CVDs. Ferroptosis is regulated by various subcellular organelles, including the plasma membrane, endoplasmic reticulum (ER), mitochondria, mitochondria-associated membranes (MAMs), peroxisomes, lysosomes, Golgi apparatus, lipid droplets, and nucleus. The plasma membrane rupture is a key event in ferroptosis, and the ER is involved in the regulation of ferroptosis through ER stress and the unfolded protein response. Mitochondria play a central role in ferroptosis, as they are the main source of ROS and are involved in iron metabolism. MAMs are involved in the trafficking of phosphatidylserine into mitochondria and phosphatidylethanolamine out of mitochondria, acting as a mechanical link between ER and mitochondria. Peroxisomes produce ROS and reactive nitrogen species (RNS) and are involved in lipid metabolism. Lysosomes are involved in ferroptosis through autophagy, release of lysosomal cathepsin, and accumulation of lysosomal iron or nitric oxide. The Golgi apparatus processes, modifies, and packages proteins, and its dysfunction can lead to ferroptosis. Lipid droplets are storage organelles that are involved in lipid metabolism and can affect the sensitivity of cells to ferroptosis. The nucleus is involved in ferroptosis through the release of nuclear DNA and the regulation of DNA damage response pathways. The mechanisms of ferroptosis include iron regulation, amino acid metabolism, and lipid metabolism. Iron regulation is crucial for ferroptosis, as excessive iron can lead to the Fenton reaction and the production of hydroxyl radicals. Amino acid metabolism is involved in the regulation of ferroptosis through the synthesis of glutathione (GSH) and the activity of glutathione peroxidase 4 (GPX4). Lipid metabolism is involved in the regulation of ferroptosis through lipid peroxidation and the production of toxic substances such as 4-hydroxynonenal (4-HNE) and malonaldehyde (MDA). The ferroptosis inhibitory protein 1 (FSP1)-CoFerroptosis is a type of regulated cell death (RCD) that plays a significant role in the pathogenesis of cardiovascular diseases (CVDs). It is characterized by iron-dependent lipid peroxidation and the accumulation of reactive oxygen species (ROS). Ferroptosis is involved in various CVDs, including myocardial infarction, heart failure, atherosclerosis, and pulmonary arterial hypertension. The mechanisms of ferroptosis involve iron metabolism, glutathione metabolism, and lipid metabolism. Recent research has shown that ferroptosis is involved in the occurrence and development of CVDs, and understanding its mechanisms can provide new ideas and treatment targets for the clinical diagnosis and treatment of CVDs. Ferroptosis is regulated by various subcellular organelles, including the plasma membrane, endoplasmic reticulum (ER), mitochondria, mitochondria-associated membranes (MAMs), peroxisomes, lysosomes, Golgi apparatus, lipid droplets, and nucleus. The plasma membrane rupture is a key event in ferroptosis, and the ER is involved in the regulation of ferroptosis through ER stress and the unfolded protein response. Mitochondria play a central role in ferroptosis, as they are the main source of ROS and are involved in iron metabolism. MAMs are involved in the trafficking of phosphatidylserine into mitochondria and phosphatidylethanolamine out of mitochondria, acting as a mechanical link between ER and mitochondria. Peroxisomes produce ROS and reactive nitrogen species (RNS) and are involved in lipid metabolism. Lysosomes are involved in ferroptosis through autophagy, release of lysosomal cathepsin, and accumulation of lysosomal iron or nitric oxide. The Golgi apparatus processes, modifies, and packages proteins, and its dysfunction can lead to ferroptosis. Lipid droplets are storage organelles that are involved in lipid metabolism and can affect the sensitivity of cells to ferroptosis. The nucleus is involved in ferroptosis through the release of nuclear DNA and the regulation of DNA damage response pathways. The mechanisms of ferroptosis include iron regulation, amino acid metabolism, and lipid metabolism. Iron regulation is crucial for ferroptosis, as excessive iron can lead to the Fenton reaction and the production of hydroxyl radicals. Amino acid metabolism is involved in the regulation of ferroptosis through the synthesis of glutathione (GSH) and the activity of glutathione peroxidase 4 (GPX4). Lipid metabolism is involved in the regulation of ferroptosis through lipid peroxidation and the production of toxic substances such as 4-hydroxynonenal (4-HNE) and malonaldehyde (MDA). The ferroptosis inhibitory protein 1 (FSP1)-Co